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PubMed2005

Interactions between different selenium compounds and zinc, cadmium and mercury.

In this paper, we present a polarographic study of systems containing different inorganic and organic selenium compounds (sodium selenite, sodium selenate, seleno-methionine and seleno-urea) and metal ions (Zn2+, Cd2+ Hg2+) of the 12th group of elements in the periodic table. While zinc is a trace element known to be essential for plants and animals, cadmium and mercury are exogenous elements and are harmful pollutants that accumulate during aging; selenium is also recognized as an important micronutrient and is sometimes added to the diet. Experiments investigating the interactions were carried out using polarographic techniques in unbuffered systems. The three metal cations originated complexes with different strength and solubility in the presence of selenite anions; in the presence of selenate, polarography was not able to detect formation of complexes with these metal ions, at least under the experimental conditions used: a decrease of Hg2+ ion concentration was observed. Seleno-methionine did not react with Cd2+; in the presence of Zn2+, a soluble complex with a co-ordination number 1 was formed, while, again, the concentration of Hg2+ decreased in the presence of increasing concentrations of the selenium derivative. Seleno-urea did not react with Zn2+, but formed a complex with Cd2+ with limited solubility. Finally, this ligand could not be studied with Hg2+ because of the overlapping of the reduction potentials of both the ligand and the metal cation. Overall equilibrium constants for complex formation (Kf) and the solubility product (Ksp) for poorly soluble species are also reported.

Cadmium↗
PubMed1994

Induction of developmentally programmed cell death and activation of HIV by sodium butyrate.

Apoptosis is an important regulatory process during normal development and maturation. We find that the proliferation-arresting and differentiation-inducing compound sodium n-butyrate (NaB) triggers a marked host chromatin degradation. This apoptotic process is independent of, but commensurate with, a rapid increase in viral mRNA synthesis and subsequent release of HIV-1 virus in transformed human cell lines harboring tat- (HLM1) or tat+ (U1, ACH-2) dormant HIV-1 proviruses. This compound stimulates a reversible accumulation of the characteristic viral mRNAs at a much faster rate than two other DNA degradation inducers such as tumor necrosis factor-alpha and phorbol 12-myristate 13-acetate. The transcriptional activator butyrate analogue, alpha-amino-n-butyrate, failed to cause similar phenotypic changes. These results suggest that common regulatory signals may be involved in activation of apoptosis genes and latent provirus by NaB.

Apoptosis↗
PubMed1999

Hofmeister effects of anions on the kinetics of partial reactions of the Na+,K+-ATPase.

The effects of lyotropic anions, particularly perchlorate, on the kinetics of partial reactions of the Na+,K+-ATPase from pig kidney were investigated by two different kinetic techniques: stopped flow in combination with the fluorescent label RH421 and a stationary electrical relaxation technique. It was found that 130 mM NaClO4 caused an increase in the Kd values of both the high- and low-affinity ATP-binding sites, from values of 7.0 (+/- 0.6) microM and 143 (+/- 17) microM in 130 mM NaCl solution to values of 42 (+/- 3) microM and 660 (+/- 100) microM in 130 mM NaClO4 (pH 7.4, 24 degrees C). The half-saturating concentration of the Na+-binding sites on the E1 conformation was found to decrease from 8-10 mM in NaCl to 2.5-3.5 mM in NaClO4 solution. The rate of equilibration of the reaction, E1P(Na+)3 left arrow over right arrow E2P + 3Na+, decreased from 393 (+/- 51) s-1 in NaCl solution to 114 (+/- 15) s-1 in NaClO4. This decrease is attributed predominantly to an inhibition of the E1P(Na+)3 --> E2P(Na+)3 transition. The effects can be explained in terms of electrostatic interactions due to perchlorate binding within the membrane and/or protein matrix of the Na+,K+-ATPase membrane fragments and alteration of the local electric field strength experienced by the protein. The kinetic results obtained support the conclusion that the conformational transition E1P(Na+)3 --> E2P(Na+)3 is a major charge translocating step of the pump cycle.

Adenosine Triphosphate↗
PubMed1993

Nitric oxide-donating compounds stimulate electrolyte transport in the guinea pig intestine in vitro.

The role of nitric oxide (NO) as a regulator of intestinal electrolyte transport was investigated in stripped segments of guinea pig intestine mounted in Ussing chambers. Serosal application of the NO-donating compounds sodium nitroprusside or isosorbide dinitrate (in the presence of 5 microM L-cysteine) resulted in concentration-dependent increases in the short circuit current. The response to 0.5 mM nitroprusside was exhibited to the same degree in duodenum, jejunum, ileum and proximal colon, and to a lesser degree in the distal colon. The response to nitroprusside was reduced by pretreatment with either the cyclo-oxygenase inhibitor, indomethacin (45% inhibition), the 5-HT3 antagonist, BRL43694 (30% inhibition) or by incubation with chloride-free buffer (59% inhibition). There was no significant effect of the 5-HT2 receptor antagonist, LY53857, or the neural blocker, tetrodotoxin. Pretreatment of ileal segments with the NO synthase inhibitor, NG-monomethyl-L-arginine, did not significantly alter the short circuit current response to electrical field stimulation compared to controls. Exposure of ileal mucosal scrapings to sodium nitroprusside resulted in a significant increase in cGMP production. The data suggest that exogenous NO-donating compounds can modulate electrolyte transport in the guinea pig intestine in vitro. The response is cyclo-oxygenase-, 5-HT3- and chloride-dependent, and coincides with increases in mucosal cGMP. However, the role of endogenous NO in regulating electrolyte transport remains unclear.

Amino Acid Oxidoreductases↗
PubMed1989

Dithiocarbamate-induced biliary platinum excretion and the control of cis-platinum nephrotoxicity.

Treatment with any one of six different dithiocarbamates subsequent to the administration of cis-platinum (CDDP) is shown to promote the biliary excretion of platinum. The administration of the most effective of these compounds, sodium diethyldithiocarbamate (DDTC) at 1.57 mmol/kg, led to a 30-fold increase in the biliary excretion of platinum. For the other dithiocarbamates investigated, a similar dosage led to increases ranging from approximately 5-fold for sodium iminodiacetic acid dithiocarbamate, to 26-fold for sodium sarcosine dithiocarbamate. The presence of alkyl groups on the nitrogen of the dithiocarbamate increased the effectiveness of the compounds. There is no increase in the platinum levels of the brain when DDTC is used in this manner. A histopathological evaluation of the kidneys of rats given 15 mg CDDP/kg in 6.3% saline with and without the use of dithiocarbamates for renal protection shows significant additional protection due to the use of the dithiocarbamates. Dithiocarbamates given at an appropriate dosing schedule can lead to a significant reduction in the renal damage which is revealed by microphotographs. It is suggested that part of the renal protection obtained by the use of dithiocarbamates may be due to this shift of platinum excretion to the bile which obviates additional renal exposure to platinum. It was also found that the simultaneous injection of a dithiocarbamate with the cis-platinum has no obvious effect on the anti-cancer action of cis-platinum against the Walker 256 carcinosarcoma in rats.

Animals↗
PubMed2006

Genotoxic and antigenotoxic properties of selenium compounds in the in vitro micronucleus assay with human whole blood lymphocytes and TK6 lymphoblastoid cells.

Selenium is known to possess both genotoxic and antigenotoxic properties. In the present study, we have evaluated the genotoxicity and antigenotoxicity of three selenium compounds (sodium selenate, sodium selenite and selenous acid) by measuring in vitro micronucleus induction. Assays were conducted in whole blood lymphocytes and in the TK6 lymphoblastoid cell line, with and without co-treatment with potassium dichromate, a known genotoxic compound. In general, the compounds were more active in TK6 cells than they were in blood lymphocytes. Only 1 microM selenous acid increased the frequency of binucleated cells containing micronuclei (BNMN) in blood lymphocytes, while all three selenium compounds increased BNMN in TK6 cells. In addition, combinations of selenous acid and potassium dichromate resulted in lower frequencies of BNMN than potassium dichromate alone in blood lymphocytes, while combinations of sodium selenate and potassium dichromate produced lower frequencies of BNMN than potassium dichromate alone in TK6 cells. The concentrations of selenium compounds that were used, in combination with the medium components and the biological physiology of the whole blood lymphocytes and TK6 cells, could have affected the redox potential of the compounds, switching the chemicals from a pro-oxidant to antioxidant status and vice-versa. The lower activities of the compounds in blood lymphocytes may be due to the protective effects of blood components. The results indicate that the genotoxic and antigenotoxic properties of selenium compounds are highly dependent upon the conditions under which they are evaluated.

Adult↗
PubMed2001

Analytical control of a pharmaceutical formulation of sodium picosulfate by capillary zone electrophoresis.

A new procedure for the analytical control of a pharmaceutical formulation by capillary zone electrophoresis (CZE) is proposed. It allows the simultaneous determination of the major compounds in the formulation: active compound (sodium picosulfate) and preservative (methylparaben), and the degradation products of the preservative, which slowly degrades by hydrolysis or by transesterification with sorbitol (sweetener in excess in the formulation) yielding p-hydroxybenzoic acid and sorbitolparaben, respectively. UV-Vis detection in the absorption maxima of the analytes and 20 mM borate solution at pH 10 as background electrolyte are used. Results are compared with those provided by the HPLC procedure. The method has also been validated using the HPLC procedure as the reference method, evaluating selectivity, accuracy, linearity and precision. The CZE procedure developed is sufficiently accurate and the precision achieved is about 1% for major and 3% for minor compounds.

Calibration↗
PubMed1995

Sodium nitroprusside induces internalization of muscarinic receptors stably expressed in Chinese hamster ovary cell lines.

We have characterized the internalization of muscarinic acetylcholine receptors induced by the nitric oxide (NO)-generating compound sodium nitroprusside. When Chinese hamster ovary cells, stably transfected with the human m4 muscarinic receptor subtype, were incubated for 1 h in the presence of 700 microM sodium nitroprusside, the number of receptors measured in intact cells with the hydrophilic ligand N-[3H]methylscopolamine was reduced by 30%. The effect was dose dependent, beginning with a concentration of sodium nitroprusside as low as 45 microM. Removal of sodium nitroprusside from the incubation medium did not result in a recovery of the binding sites. The phenomenon was temperature dependent and was blocked by the muscarinic antagonist atropine. No receptor diminution was detected when the number of binding sites was evaluated with the lipophilic antagonist [3H]quinuclidinyl benzilate. This indicates that sodium nitroprusside induces a redistribution of the muscarinic receptors between the plasma membrane and an internal compartment of the cell. Receptor loss was readily reversed by treatment with the sulfhydryl reducing agent diethyldithiocarbamate. Our data provide evidence that muscarinic receptors are internalized by sodium nitroprusside through the oxidation of sulfhydryl groups; they also suggest that NO could play a role in muscarinic receptor desensitization.

Animals↗
PubMed1988

Effects of various vanadium compounds on cochlear potentials.

The effects of vanadium compounds, sodium vanadate, ammonium vanadate, potassium vanadate, vanadium oxysulfate, vanadium acetylacetonate, and vanadium trichloride, on endocochlear potential (EP) and cochlear microphonic potential (CM) were examined in the guinea pig cochlea. The perilymphatic space was perfused for 30 min with 1 mM solution of each compound and changes of EP, CM, and negative EP were observed. Upon perfusion with pentavalent vanadium solutions, such as sodium vanadate, ammonium vanadate, and potassium vanadate, the EP showed an overshoot at the beginning of perfusion and then a gradual decrease, while the CM showed only a gradual decrease. The other compounds had no effects on EP and CM. Since the negative EP showed no differences due to perfusion of any compound, it is concluded that the vanadate compounds have inhibitory effects on EP primarily, and on CM only secondarily. The chemical mechanism of the effects of vanadates was discussed concerning the function of the stria vascularis and also its participation in acute hearing loss.

Animals↗
PubMed1987

The synthesis of some branched-chain-sugar nucleoside analogues.

1-(2,3-Epoxy-5-O-trityl-beta-D-lyxofuranosyl)uracil was treated with a number of carbon nucleophiles. Ethynyl lithium gave 3'-deoxy-3'-ethynyl-5'-O-trityl-ara-uridine, which was reduced to the corresponding 3'-ethenyl compound. Sodium cyanide gave 3'-cyano-3'-deoxy-5'-O-trityl-ara-uridine which upon alkaline hydrolysis gave the corresponding 3'-carboxamido compound. 1,3-Dithian-2-yl lithium gave 3'-deoxy-3'-(1,3-dithian-2-yl)-5'-O-trityl-ara-uridine. The trityl group was removed from each of these compounds by mild acidic hydrolysis. Treatment of 2 with 0.1M H2sO4 and mercury (II) acetate afforded 3'-acetyl-3'-deoxy-ara-uridine which upon reduction with NaBH4 gave 3'-deoxy-3'-(1-hydroxyethan-1-yl)-ara-uridine. Acetylation of 6 yielded 5'-O-acetyl-3'-acetyl-2',3'-didehydro-2',3'-dideoxyuridine which upon reduction with NaBH4 produced a mixture of 5'-O-acetyl-2',3'-didehydro-2',3'-dideoxy-3'-(1-hydroxyethan -1-yl)uridine and 1-(R)[5-(S)-acetoxymethyl-4-(1-hydroxyethan-1-yl)-tetrahydrofuran- 2-yl]- uracil. Reduction of 14 with Raney nickel followed by removal of the trityl group gave 3'-deoxy-3'-methyl-ara-uridine.

Indicators and Reagents↗
PubMed2004

Efficacy of egg cleaning compounds on eggshells contaminated with Salmonella enterica serovar Enteritidis.

Salmonella Enteritidis infections of egg contents can be related to external contamination of the shell. In this study, the efficacy of three commercial cleaning and/or sanitizing compounds (sodium carbonate, sodium hypochlorite, and potassium hydroxide) was evaluated for bactericidal activity at pH values of 10, 11, and 12 against various concentrations (10(2), 10(4), or 10(6) CFU/ml) of Salmonella Enteritidis inoculated onto the eggshell surface. Efficacy of these chemical agents was also assessed against Salmonella Enteritidis in aqueous suspension. Our results indicated that none of the chemicals applied at the recommended manufacturer's concentrations (sodium carbonate, 36 ppm; other treatments, 200 ppm) could eliminate Salmonella Enteritidis from eggshells artificially contaminated with the highest bacterial concentrations (10(4) or 10(6) CFU/ml). Higher concentrations of each product, at least 5 to 20 times greater than recommended doses, were needed to destroy the bacteria on egg surfaces. However, at or slightly above the manufacturer's recommended use concentrations, all three formulations were effective against Salmonella Enteritidis in aqueous suspension (10(8) CFU/ml) or on eggshells contaminated with 10(2) CFU/ml. For both shell and suspension assays, inactivation of Salmonella Enteritidis occurred at lower concentrations at pH 12 than at pH 11 and 10. Contact time between chemicals and Salmonella apparently influenced bacterial inactivation. Extended contact times (2 to 10 min) reduced minimum chemical concentrations necessary to inactivate the bacteria. However, neither pH nor contact time influenced Salmonella Enteritidis inactivation when the initial bacterial numbers on eggshells were high.

Animals↗
PubMed1989

Sodium thiosulfate inhibits cisplatin-induced mutagenesis in somatic tissue of Drosophila.

The antitumor agent cisplatin was evaluated for genotoxicity in the somatic tissue of Drosophila melanogaster in combination with the nucleophilic compound sodium thiosulfate (STS). Third instar larvae transheterozygous for mwh and flr3 were grown on media containing (1) water, (2) 200 mM STS, (3) 0.05 mM cisplatin in 200 mM STS, or (4) 0.05 mM cisplatin. Wings of surviving adults were scored for the presence of twin spots and both small and large single spots; 200 mM STS was nongenotoxic in the assay. Whereas 0.05 mM cisplatin significantly induced all three endpoints, 0.05 mM cisplatin in combination with 200 mM STS was found to have no genotoxic activity. Hence, STS possessed antimutagenic activity in the wing-spot assay and completely inhibited cisplatin-induced mutagenesis and mitotic recombination.

Animals↗
PubMed2003

Poly[sodium(I)-micro(6)-hydrogen benzene-1,4-dicarboxylato].

Alkali metal salts of terephthalic acid are common reagents in the preparation of metal-ligand coordination complexes containing terephthalate anions. In the title compound, sodium hydrogen terephthalate, [Na(C(8)H(5)O(4))](n), the cations occupy crystallographic inversion centres, and each bridging anion coordinates to six octahedral cations and vice versa. As seen in the known potassium derivative [Kaduk (2000). Acta Cryst. B56, 474-485; Miyakubo, Takeda & Nakamura (1994). Bull. Chem. Soc. Jpn, 67, 2301-2303], sodium hydrogen terephthalate contains short O-H.O hydrogen bonds between anions [O.O = 2.4734 (17) A]. The structure is centrosymmetric and exhibits disorder of the H-atom position in the hydrogen bond and of the non-bridging ring C atoms in the terephthalate ion.

Journal Article↗
PubMed1975

Surface and solution properties of steroid antibiotics: 3-acetoxylfusidic acid, cephalosporin P1 and helvolic acid.

The colloid/chemical properties of the fusidane antibiotics, 3-acetoxylfusidic acid, cephalosporin P1, and helvolic acid, and their sodium salts, were investigated. The sodium salts of 3-acetoxylfusidic acid and cephalosporin P1 were found to be detergent-like molecules with micellar properties comparable to the parent compound sodium fusidate and the bile salt sodium cholate. Critical micellar temperatures (cmt) were less than 0 degrees C except for sodium helvolate which being sparingly soluble did not form micelles between 0 and 50 degrees C. Potentiometric titrations of dilute solutions gave apparent pK values (5.2-6.5) in the range expected for carboxylated steroid detergents. The apparent pK values increased significantly once the detergent concentration exceeded the critical micellar concentration (cmc). Micellar properties were determined by surface tension, titration with a water-soluble dye (Rhodamine 6G), light scattering, and solubilization of lecithin and cholesterol. Cmc's, in the range of 1.5 to 5.6 mM, were found which varied slightly depending on the method employed and in all cases fell slightly in the presence of added NaCl. The number of monomers per micelle (aggregation number) in concentrations well above the cmc was extrapolated from Debye light scattering plots in 0.15 M NaCl. The values varied from 6 for fusidate to 14 for 3-acetoxylfusidate with sodium cephalosporin P1 having an intermediate value. Each detergent readily solubilized the phospholipid lecithin.

Cephalosporins↗
PubMed1992

Sodium stibogluconate (Pentostam) overdose during treatment of American cutaneous leishmaniasis.

A 27-year-old woman who acquired cutaneous leishmaniasis in Central America was inadvertently treated with 10 times the intended daily dose of the pentavalent antimonial compound sodium stibogluconate (Pentostam): 8500 mg (143 mg/kg) instead of 850 mg. The patient felt "wiped out" during the 4-h infusion of the drug. After the mistake in dosing was discovered, she was vigorously hydrated and carefully monitored in an intensive care unit for greater than 48 h. Her vital signs were stable, and no arrhythmias were noted. Her alanine aminotransferase level rose briefly to 2.4 times the upper limit of normal, and her white blood cell count briefly fell 43% to a low of 3700/microliter. Her skin lesions subsequently healed without further therapy. Although sodium stibogluconate has been associated with a variety of side effects, in this case, a single high dose of the drug was tolerated without serious toxicity.

Adult↗
PubMed2004

[The effect of all-trans retinoid acid and sodium selenite (Na2SeO3) on VEGF and its receptor expression in HL-60 cells].

In order to investigate the effect of non-medullar toxicity drug - all trans retinoid acid (ATRA) and cancer preventive trace element-selenium compound - sodium selenite (Na(2)SeO(3)) on the expression of vascular endothelial growth factor (VEGF) and its receptor in HL-60 cells, the expression of VEGF and its receptor in HL-60 cells were detected by ELISA technique and flow cytometry before and after treatment with two drugs. The results showed that the mean VEGF concentrations in the cultural supernatant of 5 and 10 micro mol/L ATRA-treated HL-60 cells for 48 and 72 hours were lower than those of the control group without adding ATRA. The differences between the ATRA-treated groups and the control group were statistically significant (P = 0.001, P = 0.000, P < 0.01, respectively). The levels of VEGF-R on the surface of HL-60 cells also decreased after treatment with ATRA of 5 and 10 micro mol/L for 72 hours, but at 48 hours the expression rates of VEGF-R on HL-60 cells of the two ATRA treated groups were not significantly decreased. At 48 and 72 hours, Na(2)SeO(3) of 5 and 10 micro mol/L had no obvious effect on HL-60 secreting VEGF, but notablely inhibited the expression of VEGF-R. In conclusion, ATRA could inhibit the expression of VEGF and its receptor in HL-60 cell. Na(2)SeO(3) could not inhibit the expression of VEGF in HL-60 cell, but could decrease the receptor expression of VEGF, which mechanism should be further studied. ATRA and Na(2)SeO(3) had not obvious medullar-inhibition, but anti-angiogenesis activity. It is suggested that combination of two drugs with conventional therapy may enhance the effect of radiotherapy and chemotherapy, and reduce the dose and thus toxicity of chemotherapeutic agents.

Dose-Response Relationship, Drug↗
PubMed2000

The constituents of the root and stem of Aristolochia heterophylla Hemsl.

Seven new compounds, sodium aristolochate-VII (1), aristolactam-CIV (2), madolin-I (3), -J (4), -K (5), -L (6) and -M (7) together with 71 known compounds were isolated and characterized from the fresh root and stem of Aristolochia heterophylla Hemsl. Their structures were determined by spectral methods. Compound 8 was revised as aromadendrane-4beta, 10beta-diol by spectral data and single-crystal X-ray analysis.

Crystallography, X-Ray↗
PubMed1996

Teratogenic effects of selenium compounds on cultured postimplantation rat embryos.

Embryonic susceptibility to selenium (Se) teratogenicity was examined in rats using postimplantation embryo culture. Rat embryos at day 9.5 of gestation were cultured by the roller bottle method for 48 hr in the presence of Se compounds. Sodium selenite, sodium selenate, seleno-DL-methionine, and seleno-DL-cystine were embryolethal at 20, 300, 1,000, and 1,000 microM Se, respectively. All of these compounds caused abnormalities such as deformed optic vesicle and swollen rhombencephalon in the viable embryos. These abnormalities were considered to correspond to in vivo malformations caused by Se in hamster fetuses or in bird embryos. These results indicate that rat embryos are susceptible to Se teratogenicity. It seems that there are differences in potency ranking of Se compounds between rat and bird embryos.

Abnormalities, Drug-Induced↗